Role of calcium in acute stimulated release of prolactin from neoplastic GH3 cells.
Using a calcium-sensitive electrode to monitor calcium movements, we found that neoplastic GH3 cells experienced a net accumulation of calcium when exposed to elevated (50 mM) K+. Acute prolactin (PRL) release was also stimulated under these conditions. Both calcium uptake and PRL release could be blocked by the calcium antagonist methoxyverapamil (D-600). Thyrotropin-releasing hormone (TRH) also stimulated PRL release but had no effect on cellular calcium accumulation. Likewise, D-600 had no effect on TRH-induced PRL release. Such results indicate that enhanced secretory activity does not require an increase in intracellular calcium content. The observation that secretagogues do not stimulate PRL release in the absence of extracellular calcium was investigated. When GH3 cells were placed in a Ca-free medium, they underwent a prompt and sustained loss of cellular calcium. The loss of such intracellular calcium could be blocked with D-600. We conclude that the inability of TRH to stimulate the release of PRL in Ca-free medium is due to the loss of intracellular calcium and not to the absence of external calcium per se.
D000818:Animals; D002118:Calcium / Q000378:metabolism*; D002460:Cell Line; D005711:Gallopamil / Q000494:pharmacology; D007700:Kinetics; D010911:Pituitary Neoplasms / Q000378:metabolism*; D011188:Potassium / Q000494:pharmacology; D011388:Prolactin / Q000378:metabolism*; D051381:Rats; D013973:Thyrotropin-Releasing Hormone / Q000494:pharmacology
D005711:Gallopamil; D013973:Thyrotropin-Releasing Hormone; D011388:Prolactin; D011188:Potassium; D002118:Calcium